Stress is a common cause of various diseases. Pregnant women are highly vulnerable to a stressful environment. Several recent observational studies have consistently pointed out that prenatal maternal stress can affect allergic diseases in their offspring. Controlled animal studies have suggested possible mechanisms underlying this relationship. More substantial evidence is needed directly from human biologic samples derived from birth cohort participants demonstrating the prenatal stress- offspring allergic disease relationship.

In a report recently published in The Journal of Allergy & Clinical Immunology (JACI), Chang, Suh and colleagues analyzed two independent prospective birth cohorts (COCOA and PSKC) on the relationship between prenatal stress and the cumulative hazard for physician-diagnosed atopic dermatitis. To find additional clues that the fetuses of prenatally distressed mothers chronically were exposed to stress, glucocorticoids and increased oxidative stress, the authors further measured placental 11beta-hydroxysteroid dehydrogenase (HSD2) activity and glutathione levels in a subgroup of COCOA participants.

The first part of their research was the verification of an epidemiological association. The researchers found both cohorts consistently indicated that maternal prenatal distress is significantly associated with risk of atopic dermatitis and higher scores of maternal distress directly increased the predicted probability of AD development in offspring. This relationship remained significant when confounding factors including postnatal stress were adjusted. Their second part of the research was the analysis of biologic samples. The researchers reported that children with distressed mothers had lower placental HSD2 activity, which could expose the fetus to excessive cortisol levels, and lower glutathione/GSSG ratios, which indicate glutathione depletion and oxidative stress induction. Moreover, the authors also found that children in the group of distressed mothers and later developed atopic dermatitis had the highest 1-year-old serum total IgE levels.

This work provides clues suggesting a chronic stress-steroid-reactive oxygen species mechanism for the development of atopic dermatitis in children by investigating placental samples as well as their epidemiological data from a purposely-designed birth cohort.

The Journal of Allergy and Clinical Immunology (JACI) is the official scientific journal of the AAAAI, and is the most-cited journal in the field of allergy and clinical immunology.